Frequent premature atrial contractions as a signalling marker of atrial cardiomyopathy, incident atrial fibrillation, and stroke

Abstract

Premature atrial contractions are a common cardiac phenomenon. Although previously considered a benign electrocardiographic finding, they have now been associated with a higher risk of incident atrial fibrillation (AF) and other adverse outcomes such as stroke and all-cause mortality. Since premature atrial contractions can be associated with these adverse clinical outcomes independently of AF occurrence, different explanations have being proposed. The concept of atrial cardiomyopathy, where AF would be an epiphenomenon outside the causal pathway between premature atrial contractions and stroke has received traction recently. This concept suggests that structural, functional, and biochemical changes in the atria lead to arrhythmia occurrence and thromboembolic events. Some consensus about diagnosis and treatment of this condition have been published, but this is based on scarce evidence, highlighting the need for a clear definition of excessive premature atrial contractions and for prospective studies regarding antiarrhythmic therapies, anticoagulation or molecular targets in this group of patients.

Keywords: Anticoagulation; Atrial cardiomyopathy; Atrial myopathy; Premature atrial contractions; Stroke; Supraventricular ectopic beats.

Graphical Abstract

The concept of atrial cardiomyopathy and its association with atrial ectopy, atrial fibrillation, and stroke. Atrial cardiomyocytes and non-cardiomyocyte elements react briskly and extensively to pathological stimuli and are susceptible to a range of genetic influences, leading to structural, functional, and biochemical changes that will have a substantial impact on cardiac performance, arrhythmia occurrence, and stroke risk. Created with figures from BioRender.com. CRP, C-reactive protein; IL-6, interleukin 6; TNF-α, tumour necrosis factor alpha; vWF, von Willebrand factor.

Figure 1

Atrial cells reaction to pathological stimuli, leading to a hypercoagulable state. Atrial cells react to pathological stimuli by cardiomyocyte changes, fibroblast proliferation, interstitial fibrosis, release of pro-inflammatory cytokines and hormones, release of reactive oxygen species, and expression of prothrombogenic factors. Created with BioRender.com. ANP, atrial natriuretic peptide; IL-6, interleukin 6; NF-kB, nuclear factor kappa-light-chain-enhancer of activated B cells; NO, nitric oxide; ROS, reactive oxygen species; TNF-α, tumour necrosis factor alpha; vWF, von Willebrand factor.